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Biomedical subjects

J A Lang

Publications and source records attributed to J A Lang.

17 recordsLinked to original sources
PubMed1999

Changes in gastric contents in pigs fed a finely ground and pelleted or coarsely ground meal diet.

The objective was to characterize the change in stomach contents in relation to time after feeding between pigs consuming a restricted amount of a finely ground and pelleted (FGP) or coarsely ground meal (CGM) diet. Particular interest was placed on the concentration of organic acids and ammonia, the products of microbial fermentation. Thirty barrows were ranked by weight and assigned to a postfeeding time of 2, 4, 6, 8, or 12 h and either the FGP or CGM diet. Initiation and termination of the experiment were staggered over a 2-wk period. The treatment period was 42 d. Percentage of dry matter was higher (P<.01) in the stomach contents of pigs on the CGM diet. Concentrations of pepsin and protein were higher (P<.05) and ammonia tended to be higher (P = .10) in the proximal stomach of pigs fed the FGP diet. In contrast, concentrations of acetate and L-lactate were higher (P<.05) in the proximal stomach of pigs fed the CGM diet. All pigs on the CGM diet had stomachs that graded as normal on visual inspection. There was variable damage to the stomachs of pigs on the FGP diet. Measurement of chromium concentration in the stomach after an oral dose of Cr-EDTA clearly demonstrated the mixing that occurs between the proximal and distal stomach by 2 h after feeding in pigs consuming the FGP diet, whereas a gradient was maintained in pigs consuming the CGM diet. Thus, components normally secreted in the distal stomach return to the proximal stomach. These data show that components secreted in the distal region, such as acid and pepsin, may play a role in initiating damage to the stratified squamous mucosa. High concentrations of organic acids in the stomach of pigs on the CGM diet were not associated with damage to the stratified squamous mucosa in the esophageal region.

Ammonia↗
PubMed1998

Transforming growth factor beta1 regulates the expression of cyclooxygenase in cultured cortical astrocytes and neurons.

The hypothesis that transforming growth factor beta1 (TGFbeta1) regulates the synthesis of prostaglandins by CNS tissue was tested by using purified cultures of cortical astrocytes or neurons that were obtained from rat pups on postnatal day 4 or 5 or fetuses on gestational day 16, respectively. The cells were exposed to TGFbeta1 for 2 days. The synthesis of prostaglandins depends upon the production and conversion of arachidonic acid, steps that are catalyzed by phospholipase A2 (PLA2) and cyclooxygenase (COX), respectively. Prostaglandin E2 (PGE2) concentration was determined by radioimmunoassay. The expression of cytosolic PLA2 and COX (the constitutive COX1 and the inducible COX2) was assessed by using immunohistochemical and quantitative immunoblotting procedures. Astrocytes produced much more PGE2 than neurons, suggesting that glial cells are an important source of PGE2 in the CNS. TGFbeta1 increased the production of PGE2 by astrocytes and neurons in a concentration-dependent manner. Furthermore, TGFbeta1 enhanced COX activity; the inhibitor indomethacin completely blocked TGFbeta1-mediated PGE2 synthesis. Cultured astrocytes and neurons expressed the three enzymes: cytosolic PLA2, COX1, and COX2. Cytosolic PLA2 expression was unaffected by TGFbeta1 treatment. In contrast, COX expression was altered by TGFbeta1 treatment in a concentration-dependent fashion. COX1 was increased by TGFbeta1, but only in astrocytes. TGFbeta1 increased COX2 expression in astrocytes and neurons. Thus, TGFbeta1-induced increases in PGE2 concentration are regulated by COX. This study suggests that TGFbeta1 is an important regulator of immune and inflammatory processes in the CNS.

Animals↗
PubMed1996

Arterial oxygen saturation in healthy term neonates.

UNLABELLED: Our objective was to determine arterial oxygen saturation as measured by pulse oximetry (SpO2) in healthy term neonates during their first 4 weeks of life. Overnight recordings of SpO2 (Nellcor N200), photoplethysmographic (pulse) waveforms from the oximeter and breathing movements were performed in 60 term infants. They were studied initially during their 1st week of life (median age 4 days, range 1-7) and then again during their 2nd-4th week (median age 17 days, range 8-27). Median baseline SpO2, measured during regular breathing, was 97.6% (range 92-100) during week 1 versus 98.0% (86.6-100) during week 2-4 (P > 0.05). Episodes of desaturation, defined as a fall in SpO2 to < or = 80% for > or = 4 s, were found in 35% of recordings obtained in week 1 compared to 60% of those obtained in week 2-4 (P < 0.01). Their frequency increased from a median of (0-41) per 12 h of recording at the initial recording to 1 (0-165) at follow up (P < 0.01). Analysis of the data by week of life showed a peak in desaturation frequency in the 2nd week of life. The infants with extreme values at follow-up (e.g. a baseline SpO2 of 86.6%, 5th percentile 91.9%, or a desaturation frequency of 165 per 12 h of recording, 95th percentile 32) had had values well within the normal range during their initial recording (a baseline SpO2 of 94.4%, or a desaturation frequency of 4). Most of the desaturations in the infants with extreme values were associated with periodic apnoea. These results demonstrate only relatively minor developmental changes in oxygenation in term neonates during the first 4 weeks of life. The clinical significance of outlying values, i.e. a low baseline SpO2 or a high number of episodic desaturations, remains to be determined. CONCLUSION: These healthy term neonates had values for baseline oxygen saturation and desaturation frequency that were not substantially different from those observed in older infants.

Female↗
PubMed1996

Transcriptional and posttranscriptional mechanisms regulate human renin gene expression in Calu-6 cells.

We have recently identified a human pulmonary carcinoma cell line (Calu-6) that expresses human renin (hREN) mRNA endogenously, and we use it herein as a model to examine the regulation of the hREN gene. Transfection analysis of a deletion series (-2750 to -149) of hREN promoter-luciferase fusion constructs revealed the presence of multiple weak regulatory elements within the first 1,301 bp of the 5'-flanking region and a classic silencer element within the first intron (intron A) of the gene. The 5'-flanking regulatory domain consisted of three closely linked elements, two negative and one positive, each contributing a cell-specific threefold modulation of transcriptional activity. Treating Calu-6 cells with forskolin caused a 100-fold increase in steady-state endogenous hREN mRNA but no increase in hREN promoter activity in transient transfections or in nuclear runoff transcription assays. Nevertheless, de novo transcription and translation were necessary for adenosine 3',5'-cyclic monophosphate (cAMP)-mediated induction. Our results suggest that multiple regulatory elements regulate basal transcriptional activity of the hREN gene and the increase in hREN mRNA by cAMP may be mediated by posttranscriptional mechanisms.

Base Sequence↗
PubMed1995

Endogenous human renin expression and promoter activity in CALU-6, a pulmonary carcinoma cell line.

We have previously reported that transgenic mice containing the human renin gene express high levels of human renin mRNA in the lung. We show in this report that human renin expression in two lines of transgenic mice is developmentally regulated. Human renin expression is not evident in the transgenic mouse lung at 15.5 days of gestation, is detectable at 17.5 days of gestation, peaks around birth, and remains elevated into adulthood. In situ hybridization of mouse fetal lung samples at 18.5 days of gestation revealed that human renin was exclusively expressed in pulmonary type II epithelial cells. A survey of the medical literature revealed a number of clinical cases in which hypertension was caused by renin-secreting pulmonary tumors and a fairly widespread occurrence of immunoreactive renin in banked pulmonary tumors of diverse origin. This prompted us to examine a number of pulmonary tumor cell lines to determine whether they express human renin mRNA. One pulmonary carcinoma cell line, CALU-6, expressed human renin mRNA endogenously. Human renin expression in these cells was induced approximately 100-fold after treatment with forskolin, 8-bromoadenosine 3':5'-cyclic monophosphate, or N6,2'-O-dibutyryladenosine 3':5'-cyclic monophosphate. Transfection analysis of human renin promoter-luciferase fusion constructs revealed the presence of cell-specific positive and negative regulatory elements in the human renin 5'-flanking DNA. This cell line is the only immortalized human cell line that expresses high levels of endogenous human renin mRNA and should provide an excellent tool for studying the regulation of human renin expression in vitro.

Animals↗
PubMed1995

Tissue-specific expression of novel messenger ribonucleic acids cloned from a renin-expressing kidney tumor cell line (As4.1).

As4.1 cells are derived from a renin-expressing kidney tumor induced by tissue-specific oncogene-mediated tumorigenesis in transgenic mice. These cells express high levels of renin messenger RNA (mRNA) and synthesize prorenin and renin; they were therefore used as a model to further investigate the molecular biology of renin-producing kidney cells by cloning and characterizing novel mRNAs expressed in these cells. One clone, designated 1.5, was randomly selected from an As4.1 complementary DNA (cDNA) library, and two other cDNA clones, designated 4.9 and 6.9, were obtained by screening the cDNA library using a strategy to identify As4.1 cell-specific mRNAs. Each clone exhibited a highly restricted tissue-specific expression profile, including high level expression in As4.1 cells and low level expression in kidney. No homology was found between the sequence of the partial 1.5 and 4.9 cDNAs and sequences in Genbank. Southern blot analysis revealed that clone 4.9 is encoded by a single copy gene containing at least two separate exons. A homology search of the sequence of clone 6.9 revealed it to encode a cDNA to serum amyloid A protein; consistent with this identification, expression of 6.9 mRNA was highly induced in both kidney and liver after treatment of mice with Escherichia coli lipopolysaccharide.

Animals↗
PubMed1995

Human renin 5'-flanking DNA to nucleotide-2750.

Renin is one of the most important factors in blood pressure and electrolyte regulation in mammals and the renin locus has been implicated in hypertension. To assist studies of promoter control we therefore determined the 5'-flanking sequence of the human gene (REN) to residue -2750 relative to the transcription start site (+1). Sites of homology to consensus sequences for binding of trans-acting factors involved in transcriptional control of other genes were identified, and functionality for two of these (a CRE and Pit-1 site) have so far been demonstrated.

Base Sequence↗
PubMed1992

Regulated tissue- and cell-specific expression of the human renin gene in transgenic mice.

Transgenic mice containing the human renin gene were constructed with the aim of examining the tissue- and cell-specific expression of human renin. The human renin transgene used consisted of a genomic sequence extending approximately 900 bp upstream and 400 bp downstream of the coding region and included all exon and intron sequences. Two assays were developed to differentiate human renin transcripts from endogenous mouse renin transcripts at the whole-tissue level. High level human renin expression was evident in the kidney, adrenal gland, ovary, testis, lung, and adipose tissue of all four transgenic lines examined. Human renin mRNA could also be detected at lower levels in the submandibular gland and heart of two different individual lines. No expression was evident in the liver or brain of any line tested. In situ hybridization revealed the human renin mRNA to be localized and exquisitely restricted to renal juxtaglomerular cells. Treatment of transgenic mice with captopril resulted in an increase in the accumulation of renal renin mRNAs derived from both the mouse and human renin genes. Plasma renin activity assays using synthetic human renin substrate clearly demonstrated the elaboration of active human renin into the systemic circulation of transgenic mice. These data strongly suggest that the human renin transgene exhibits both tissue- and cell-specific expression in transgenic mice. Its expression is entrained to the same regulatory signals as the endogenous renin gene in kidney, and active human renin is released into the plasma of the transgenic mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Treatment of radiation enteritis: a comparison study.

Twenty-four patients with severe radiation injury to the small bowel seen over a 4-year period were randomized to four treatment groups: 1) methylprednisolone 80 mg intravenously plus Vivonex-HN, 2 L/day po, 2) methylprednisolone 80 mg intravenously plus total parenteral nutrition, 2.5 L/day, 3) total parenteral nutrition, 2.5 L/day, and 4) Vivonex-HN, 2 L/day po. Patients received nothing by mouth except water in groups II and III, and only Vivonex-HN in groups I and IV. Patients were treated for 8-wk periods. Improvement was gauged by overall nutritional assessment measurements, nitrogen balance data and by radiological and clinical parameters. No significant difference between groups I, II, III, and IV could be found for age, sex, mean radiation dosage, time of onset after radiation therapy, or initial nutritional assessment data. Differences statistically could be found between groups II and III and I and IV regarding nutritional assessment data, nitrogen balance, radiographic and clinical parameters after therapy, with marked improvement noted in groups II and III. We conclude that a treatment regimen consisting of total parenteral nutrition and bowel rest is beneficial in the treatment of radiation enteritis. Methylprednisolone appears to enhance this effect and indeed, may be responsible for a longer lasting response.

Abdominal Neoplasms↗
PubMed1981

Cimetidine in the treatment of gastric ulcer induced by steroidal and nonsteroidal anti-inflammatory agents.

The study of a group of patients with gastric ulcers induced by anti-inflammatory agents, was undertaken in an attempt to ascertain the effectiveness of cimetidine (Tagamet) when compared with intensified doses of antacids in their treatment. Seventy patients with medication-induced benign gastric ulcers confirmed by endoscopy and biopsy were studied. The agents principally responsible were aspirin, prednisone, ibuprofen, indomethacin, and sulindac in standard pharmacologic doses. The study was carefully controlled to exclude confusing parameters. Patients were divided into two groups. Group 1 (38 patients) received cimetidine plus and antacid (Maalox). Group 11 (32 patients) received placebo tablets plus the same dose of antacid as in Group 1. All anti-inflammatory agents were discontinued and patients were instructed to avoid known gastric irritants. Treatment periods lasted six weeks. Confirmation of healing was by endoscopic evaluation. A significant difference was noted only with respect to treatment response. Twenty-five of the 38 patients (65.7%) in group 1 receiving cimetidine plus antacid had their ulcers healed within the six-week period. Only eight of the 32 patients (25%) in Group 11 receiving placebo plus antacid had ulcer healing within this period of time (P less than .001). We conclude that a regimen of cimetidine plus intensified antacid therapy is far superior to the same dose of antacid alone in the treatment of gastric ulcer induced by anti-inflammatory agents.

Antacids↗
PubMed1980

Submucous lipoma simulating carcinoma of the colon.

A 43-year-old white man who presented for evaluation of hematochezia was found to have an abdominal mass in the proximal descending colon, suggestive of carcinoma on barium enema and at colonoscopy. Surgery revealed a submucous lipoma. We report the case to show that submucous lipomas may be mistaken for carcinoma of the colon.

Adult↗
PubMed1978

Tolazamide-induced hepatic dysfunction.

A case of tolazamide-induced hepatic injury is reported. Injury was documented by abnormal liver tests, including an elevated alkaline phosphatase, 5' nucleotidase and serum glutamic oxaloacetic transaminase. Liver biopsy confirmed the degree and type of injury which consisted of severe portal inflammation, bile duct proliferation and early fibrosis. The case is reported to further establish tolazamide as a drug capable of producing hepatic injury and to report a new form of hepatic injury attributable to a sulfonylurea agent.

Adult↗
PubMed1977

Zinc requirement of the young guinea pig.

The zinc requirement and signs of zinc deficiency of the young guinea pig were investigated. One-week-old Hartley guinea pigs were fed low-zinc, semipurified diets with either 30% EDTA-treated casein or 30% EDTA-treated soybean protein as the protein source. Zinc was supplemented as ZnCO3 at 0, 3, 6, 9, 12, and 60 ppm (casein diets) and 0, 5, 10, 15, 20, and 60 ppm (soybean protein diets). Specificity of zinc deficiency was determined by rapid growth response to zinc supplementation following a 4-week period of zinc depletion. Significant growth retardation and decreased feed efficiency were seen in guinea pigs fed casein diets with 3 ppm zinc or less added, or soybean diets with 5 ppm zinc or less added. Plasma zinc concentration was significantly decreased in guinea pigs fed soybean diets supplemented with 20 ppm zinc or less. Less dramatic trends of decreased plasma zinc level were seen when low-zinc casein diets were fed. Plasma alkaline phosphatase activity showed significant decreases when 9 ppm zinc or less was added to casein diets and when 20 ppm zinc or less was added to soybean protein diets. Zinc (12 ppm) added to casein diets and 20 ppm zinc added to zinc soybean protein diets supported maximal growth rate for the 3-week duration of the feeding trials.

Age Factors↗
PubMed1977

Malabsorption in infectious mononucleosis.

A case of infectious mononucleosis, complicated by malabsorption, is presented. Malabsorption was documented by abnormal d-xylose, small bowel series, 72-hour stool fat and jejunal biopsy. Small bowel abnormalities and other gastrointestinal manifestations of infectious mononucleosis are discussed.

Adult↗